Citation

Greengard J. Clin. Toxicol. (Dekker) 1975; 8(6): 575-597.

Copyright

(Copyright © 1975, M Dekker)

DOI

10.3109/15563657508990084

PMID

1227766

Abstract

In the present state of our knowledge it must be concluded that the outstanding anatomic changes directly attributable to acute iron poisoning are in the gastrointestinal tract and the liver. Both seem to be due to the direct action of iron upon living cells. In the stomach and small bowel the changes appear to be due to the corrosive effect of the iron salt whether in solution or in tablet form. And the anion may indeed play the predominant role as demonstrated by the observation of the severe corrosive changes observed when accumulations of ferrous sulfate tablets occur in areas of the stomach or small bowel. That the mucosal barrier to iron is broken down seems incontrovertible. And it is no longer tenable to assume that the severe complications of iron poisoning are due to the local necroses in the gastrointestinal tract. The liver, being the first parenchymal organ encountered by absorbed iron, is involved to a varying degree. The anatomic changes can progress to frank necrosis in severe cases. And even in those where overt histologic damage is not demonstrable, alterations in biochemical function occur. Anatomic changes in other parenchymal organs are probably largely secondary to dehydration, shock, hemorrhage, and infection. But the possibility of disordered enzyme systems here as well must be borne in mind though so far not demonstrated. In severe cases where hemorrhages play so large a role, albeit infrequently, the specific action of iron in interference with coagulation mechanisms is of the utmost importance. The role of therapy with deferoxamine in production of shock is discussed below. In this connection breakdown of the mucosal barrier with release of apoferritin and ferritin as a hypotensive mechanism has also been suggested by Smith.

Language: en